Practices and theories

The term low-carbohydrate diet today is most strongly associated with the Atkins Diet. However, there is an array of other diets that share to varying degrees the same principles (e.g. the Zone Diet, the Protein Power Lifeplan, the Go Lower Diet and the South Beach Diet). Therefore, there is no widely accepted definition of what precisely constitutes a low-carbohydrate diet. It is important to note that the level of carbohydrate consumption defined as low-carbohydrate by medical researchers may be different than the level of carbohydrate defined by diet advisors. For the purposes of this discussion, we focus on diets that reduce (nutritive) carbohydrate intake sufficiently to dramatically reduce or eliminate insulin production in the body and to encourage ketosis (production of ketones to be used as energy in place of glucose).

Although originally low-carbohydrate diets were created based on anecdotal evidence of their effectiveness, today there is a much greater theoretical basis on which these diets rest. The key scientific principle which forms the basis for these diets is the relationship between consumption of carbohydrates and the subsequent effect on blood sugar (i.e. blood glucose) and on production of some hormones. Blood sugar levels in the human body must be maintained in a fairly narrow range to maintain health. The two primary hormones related to regulating blood sugar levels, produced in the pancreas, are insulin, which lowers blood sugar levels (among many other effects, most of considerable significance metabolically), and glucagon, which raises blood sugar levels. In general, most western diets (and many others) are sufficiently high in nutritive carbohydrates that nearly all meals evoke insulin secretion from the beta cells in the pancreas; carbohydrates which are digested to produce glucose in the blood stream are the primary control for insulin secretion. Another aspect of insulin secretion is control of ketosis; in the non-ketotic state, the human body stores dietary fat in fat cells (ie, adipose tissue) and preferentially uses glucose as cellular fuel. By contrast, low-carbohydrate diets, or more properly, diets that are very low in nutritive carbohydrates, evoke less insulin (to cover the ingested glucose in the blood stream), leading to longer and more frequent episodes of ketosis. Some researchers suggest that this causes body fat to be eliminated from the body although this theory remains, at best, controversial, if it referes to excretion of lipids (ie, fat and oil) and not to fat metabolism during ketosis.

Low-carbohydrate diet advocates in general recommend reducing nutritive carbohydrates (commonly referred to as "net carbs," i.e. grams of total carbohydrates reduced by the non-nutritive carbohydrates) to very low levels. This means sharply reducing consumption of desserts, breads, pastas, potatoes, rice, and other sweet or starchy foods. Some recommend levels as low as 20-30 grams of "net carbs" per day, at least in the early stages of dieting (for comparison, a single slice of white bread typically contains 15 grams of carbohydrate, almost entirely starch). By contrast, the U.S. Institute of Medicine recommends a minimum intake of 130 grams of carbohydrate per day (the FAO and WHO similarly recommend that the majority of dietary energy come from carbohydrates).

Low-carbohydrate diets often differ in the specific amount of carbohydrates allowed, whether certain types of foods are preferred, whether occasional exceptions are allowed, etc. Generally they all agree that processed sugar should be eliminated, or at the very least greatly reduced, and similarly generally discourage heavily processed grains (white bread, etc.). They vary greatly in their recommendations as to the amount of fat allowed in the diet although the most popular versions today (including Atkins) generally recommend at most a moderate fat intake.

Although low-carbohydrate diets are most commonly discussed as a weight-loss approach some experts have proposed using low-carbohydrate diets to mitigate or prevent diseases ranging from diabetes to cancer to epilepsy. Indeed, it has been argued by some low-carbohydrate proponents and others that it is the rise in carbohydrate consumption, especially refined carbohydrates, that has caused the epidemic levels of many diseases in modern society.

There is also a category of diets known as low-glycemic-index diets (low-GI diets) or low-glycemic-load diets (low-GL diets), in particular the Low GI Diet by Brand-Miller et al. In reality, low-carbohydrate diets can also be low-GL diets (and vice versa) depending on the carbohydrates in a particular diet. In practice, though, "low-GI"/"low-GL" diets differ from "low-carb" diets in the following ways. First, low-carbohydrate diets treat all nutritive carbohydrates as having the same effect on metabolism, and generally assume that their effect is predictable. Low-GI/low-GL diets are based on the measured change in blood glucose levels in various carbohydrates. These vary markedly in laboratory studies; for instance, cooked carrots have a glycemic index in excess of that of pure glucose. The differeneces are due to poorly understood digestive differences between foods. However, as foods influence digestion in complex ways (eg, both protein and fat delay absorption of glucose from carbohydrates eaten at the same time) it is difficult to even approximately predict the glycemic effect (eg, over time or even in total in some cases) of a particular meal.

Another related diet type, the low-insulin-index diet, is similar except that it is based on measurements of direct insulemic responses (i.e., the amount of insulin in the bloodstream) to food rather than glycemic response (the amount of glucose in the bloodstream). Although such diet recommendations mostly involve lowering nutritive carbohydrates, there are some low-carbohydrate foods that are discouraged as well (e.g., beef). Insulin secretion is stimulated (though less strongly) by other dietary intake. Like glycemic index diets, there is difficulty predicting the insulin secretion from any particular meal, due to assorted digestive interactions and so differing effects on insulin release.